Hypertensive Crisis

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Chapter 52

Hypertensive Crisis

Anish K. Agarwal, MD, MPH, Christopher J. Rees, MD and Charles V. Pollack, MA, MD, FACEP, FAAEM, FAHA

1. What is a hypertensive crisis?

The term hypertensive crisis generally is inclusive of two different diagnoses, hypertensive emergency and hypertensive urgency. Distinguishing between the two is important because they require different intensities of therapy. It should be noted that older and less specific terminology, such as “malignant hypertension” and “accelerated hypertension,” should no longer be used. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7) defines hypertensive emergency as being “characterized by severe elevations in blood pressure (more than 180/120 mm Hg), complicated by evidence of impending or progressive target organ dysfunction.” JNC-7 defines hypertensive urgency as “those situations associated with severe elevations in blood pressure without progressive target organ dysfunction.” There is no absolute value of blood pressure that defines a hypertensive urgency or emergency or separates the two syndromes. Instead, the most important distinction is whether there is evidence of impending or progressive end-organ damage, which defines an emergency, or other symptoms that are felt referable to the blood pressure.

2. How commonly do these situations occur?

It is estimated that 50 to 75 million people have hypertension and that 1% to 2% of those will have a hypertensive emergency. In the elderly (>65 years of age), essential hypertension accounts for 424,000 emergency department (ED) visits per year, with an estimated 0.5% of all ED visits attributed to hypertensive crises.

3. What are the causes of hypertensive crisis?

The most common cause of hypertensive emergency is an abrupt increase in blood pressure in patients with chronic hypertension. Medication noncompliance is a frequent cause of such changes. Blood pressure control rates for patients diagnosed with hypertension are less than 50%. The elderly and African Americans are at increased risk of developing a hypertensive emergency. Other causes of hypertensive emergencies include stimulant intoxication (cocaine, methamphetamine, and phencyclidine), withdrawal syndromes (clonidine, β-adrenergic blockers), pheochromocytoma, physiologic stress in the postoperative period (following cardiothoracic, vascular, or neurosurgical procedures), and adverse drug interactions with monoamine oxidase (MAO) inhibitors.

4. What are the common clinical presentations of hypertensive crisis?

Typical presentations include severe headache, shortness of breath, epistaxis, faintness, or severe anxiety. Clinical syndromes typically associated with hypertensive emergency include hypertensive encephalopathy, intracerebral hemorrhage, acute myocardial infarction, acute heart failure, pulmonary edema, unstable angina, dissecting aortic aneurysm, or preeclampsia/eclampsia. Note that in hypertensive emergency presentations, there is evidence of impending or progressive target organ dysfunction and that the absolute value of the blood pressure is not pathognomonic.

5. What historical information should be obtained?

A thorough history, especially as it relates to prior hypertension, is important to obtain and document, as most patients with a hypertensive emergency carry a diagnosis of hypertension and are either inadequately treated or are noncompliant with treatment.

A thorough medication history is also essential. The patient’s current medications need to be reviewed and updated to include timing, dosages, recent changes in therapy, last doses taken, and compliance. Patients should also be questioned about over-the-counter medication usage and recreational drug use because these agents may also affect blood pressure.

6. How should the physical examination be focused?

Physical examination should start with recording the blood pressure in both arms with an appropriately sized blood pressure cuff. Direct ophthalmoscopy should be performed with attention to evaluating for papilledema and hypertensive exudates. A brief, focused neurologic examination to assess mental status and the presence or absence of focal neurologic deficits should be performed. The cardiopulmonary examination should focus on signs of pulmonary edema and aortic dissection, such as rales, elevated jugular venous pressure, or cardiac gallops. Peripheral pulses should be palpated and assessed. Abdominal examination should include palpation for abdominal masses and tenderness, and auscultation for abdominal bruits.

7. What laboratory and ancillary data should be obtained?

All patients should have an electrocardiogram performed to assess for left ventricular hypertrophy, acute ischemia or infarction, and arrhythmias. Urinalysis should be performed to evaluate for hematuria and proteinuria as signs of acute renal failure. Women of child-bearing age should have a urine pregnancy test performed. Laboratory studies should include a basic metabolic profile with blood urea nitrogen (BUN) and creatinine, a urine or serum toxicology screen, and a complete blood cell count (CBC) with a peripheral smear to evaluate for signs of microangiopathic hemolytic anemia. If acute coronary syndrome is suspected, cardiac biomarkers should be assessed. Choice of radiographic studies, if any, should be based on the presentation and diagnostic considerations. A chest radiograph is often ordered to evaluate for pulmonary edema, cardiomegaly, and mediastinal widening. If there are any focal neurologic findings, a computed tomography (CT) scan of the brain should be performed to evaluate for hemorrhage.

8. What are the cardiac manifestations of hypertensive emergencies?

Cardiac manifestations of hypertensive emergency include acute coronary syndromes, acute cardiogenic pulmonary edema, and aortic dissection. The latter deserves special attention because it has much higher short-term morbidity and mortality, requires more urgent and rapid reduction in blood pressure, and also requires specific inhibition of the reflex tachycardia often associated with blood pressure–lowering agents. It is recommended that patients with aortic dissection have their systolic blood pressure reduced to at least 120 mm Hg within 20 minutes, a much more rapid decrease than is recommended for other syndromes associated with hypertensive emergency.

9. What are the central nervous system manifestations of hypertensive emergency?

Neurologic emergencies associated with hypertensive emergency include subarachnoid hemorrhage, cerebral infarction, intraparenchymal hemorrhage, and hypertensive encephalopathy. Patients with hemorrhage and infarction usually have focal neurologic findings and may have corresponding findings on head CT or magnetic resonance imaging (MRI) of the brain. Hypertensive encephalopathy is more difficult to diagnose; symptoms may include severe headache, vomiting, drowsiness, confusion, visual disturbances, and seizures; coma may ensue. Papilledema is often present on physical examination.

10. What are the renal manifestations of hypertensive emergencies?

Renal failure can both cause and be caused by hypertensive emergency. Typically, hypertensive renal failure presents as nonoliguric renal failure, often with hematuria.

11. What are the pregnancy-related issues with hypertensive emergency?

Preeclampsia is a syndrome that includes hypertension, peripheral edema, and proteinuria in women after the twentieth week of gestation. Eclampsia is the more severe form of the syndrome, with severe hypertension, edema, proteinuria, and seizures.

12. What are general issues in the treatment of hypertensive urgency?

Patients with hypertensive urgencies often have elevated blood pressure and nonspecific symptoms, but no evidence of progressive end-organ damage. These patients do not often require urgent treatment with parenteral antihypertensives. There is no evidence to suggest that urgent treatment of patients with hypertensive urgencies in an ED setting reduces morbidity or mortality. In fact, there is evidence that too-rapid treatment of asymptomatic hypertension has adverse effects. Rapidly lowering blood pressure below the autoregulatory range of an organ system (most importantly the cerebral, renal, or coronary beds) can result in reduced perfusion, leading to ischemia and infarction. It is usually appropriate in these situations instead to gradually reduce blood pressure over 24 to 48 hours. Most patients with hypertensive urgency can be treated as outpatients, but some may need to be admitted, as dictated by symptoms and situation and to ensure close follow-up and compliance. The most important intervention for hypertensive urgency is to ensure good follow-up, which helps to promote ongoing, long-term control of blood pressure. No guidelines and no evidence support a specific blood pressure target number that must be achieved in order to safely discharge a patient with hypertensive urgency.

13. What are general issues in treating hypertensive emergencies?

JNC-7 recommends that patients with hypertensive emergencies be treated as inpatients in an intensive care setting with an initial goal of reducing mean arterial blood pressure by 10% to 15%, but no more than 25%, in the first hour and then, if stable, to a goal of 160/100-110 mm Hg within the next 2 to 6 hours. This requires parenteral agents. Aortic dissection is a special situation that requires reduction of the systolic blood pressure to at least 120 mm Hg within 20 minutes. Treatment is also required to help blunt the reflex tachycardia associated with most antihypertensive agents. Ischemic stroke and intracranial hemorrhage are also special situations, and guidelines exist for the treatment of hypertension in these settings from multiple experts, including guidelines from the American Stroke Association/American Heart Association (ASA/AHA). These guidelines state that “there is little scientific evidence and no clinically established benefit for rapid lowering of blood pressure among persons with acute ischemic stroke.” Too rapid a decline in blood pressure during the first 24 hours after presentation of an intracranial hemorrhage has been independently associated with increased mortality. The overall weight of evidence currently supports only judicious use of antihypertensive agents in the treatment of acute ischemic or hemorrhagic stroke. Expert guidance is recommended, especially if fibrinolytic therapy is being considered for acute ischemic stroke.

14. What specific agents are used for treating patients with hypertensive emergencies?

Table 52-1 reviews specific agents available for use.

TABLE 52-1

PARENTERAL AGENTS FOR USE IN HYPERTENSIVE EMERGENCIES

ACS, Acute coronary syndrome; BP, blood pressure; CAD, coronary artery disease; CHF, congestive heart failure; CKD, chronic kidney disease; CO, cardiac output; CrCl, creatine clearance; CT, cardiothoracic; CVD, cardiovascular disease; HA, headache; HE, hypertensive emergency; ICP, intracranial pressure; IOP, intraocular pressure; IV, intravenous; MAOI, monoamine oxidase inhibitor; max, maximum; MI, myocardial infarction.

15. Are different agents more helpful for different clinical situations?

Table 52-2 reviews specific agents recommended for specific situations.

TABLE 52-2

SPECIFIC ANTIHYPERTENSIVE AGENTS SUGGESTED FOR SPECIFIC HYPERTENSIVE EMERGENCY SYNDROMES

Syndrome	Suggested Anti hypertensive Agents
Aortic dissection	Nitroprusside, often in combination with esmolol, labetalol Nicardipine with β-blocker β-Blocker alone
Acute pulmonary edema	Nitroglycerin preferred Fenoldopam Nicardipine Clevidipine
Acute coronary syndrome	β-Blocker Nitroglycerin Clevidipine
HE with acute or chronic renal failure	Labetalol Nicardipine Fenoldopam Clevidipine
Eclampsia	Labetalol Nicardipine Hydralazine (all in conjunction with magnesium sulfate)
Acute ischemic stroke or ICH (If expert guidance deems BP control necessary)	Nicardipine Labetalol Clevidipine
Hypertensive encephalopathy	Clevidipine Labetalol Esmolol Nicardipine Fenoldopam Nitroprusside
Adrenergic crisis with HE	Phentolamine Nitroprusside β-Blocker

β-Blocker, beta-adrenergic blocking agent; BP, blood pressure; HE, hypertensive emergency; ICH, intracerebral hemorrhage.

Bibliography, Suggested Readings, and Website

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2. Amin, A. Parenteral medication for hypertension with symptoms. Ann Em Med. 2008;51:S1–S15.

3. Elliott, W.J. Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis. 2006;48:316–325.

4. Flanigan, J.S., Vitberg, D. Hypertensive emergencies and severe hypertension: what to treat, who to treat, and how to treat. Med Clin North Am. 2006;90:439–451.

5. Gray, R.O. Hypertension. In Marx J.A., Hockberger R.S., Walls R.M., eds.: Rosen’s emergency medicine: concepts and clinical practice, ed 6, Philadelphia: Mosby, 2006.

6. Haas, A.R., Marik, P.E. Current diagnosis and management of hypertensive emergency. Semin Dial. 2006;19:502–512.

7. Hebert, C.J., Vitdt, D.G. Hypertensive crises. Prim Care. 2008;35:475–487.

8. Marik, P.E., Varon, J. Hypertensive crisis: challenges and management. Chest. 2007;131:1949–1962.

9. National Heart, Lung, Blood Institute. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7). Publication no. NIH 03-5233. Bethesda, Md: NHLBI; 2003. pp. 54–55

10. Qureshi, A.I., Bliwise, D.L., Bliwise, N.G., et al. Rate of 24-hour blood pressure decline and mortality after spontaneous intracerebral hemorrhage: a retrospective analysis with a random effects regression model. Crit Care Med. 1999;27:480–485.

11. Stewart, D.L., Feinstein, S.E., Colgan, R. Hypertensive urgencies and emergencies. Prim Care. 2006;33:613–623.

12. Strandgaard, S., Olesen, J., Skinhoj, E., et al. Autoregulation of brain circulation in severe arterial hypertension. Br Med J. 1973;1:507–510.

13. Zampaglione, B., Pascale, C., Marchisio, M., et al. Hypertensive urgencies and emergencies: prevalence and clinical presentation. Hypertension. 1996;27:144–147.

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